Neuroimaging findings in newborns with congenital heart disease prior to surgery: an observational study

Abstract

ObjectivesNeurodevelopmental impairment has become the most important comorbidity in infants with congenital heart disease (CHD). We aimed to (1) investigate the burden of brain lesions in infants with CHD prior to surgery and (2) explore clinical factors associated with injury.Study designProspective observational study.SettingSingle centre UK tertiary neonatal intensive care unit.Patients70 newborn infants with critical or serious CHD underwent brain MRI prior to surgery.Main outcome measuresPrevalence of cerebral injury including arterial ischaemic strokes (AIS), white matter injury (WMI) and intracranial haemorrhage.ResultsBrain lesions were observed in 39% of subjects (95% CI 28% to 50%). WMI was identified in 33% (95% CI 23% to 45%), subdural haemorrhage without mass effect in 33% (95% CI 23% to 45%), cerebellar haemorrhage in 9% (95% CI 4% to 18%) and AIS in 4% (95% CI 1.5% to 12%). WMI was distributed widely throughout the brain, particularly involving the frontal white matter, optic radiations and corona radiata. WMI exhibited restricted diffusion in 48% of cases. AIS was only observed in infants with transposition of the great arteries (TGA) who had previously undergone balloon atrial septostomy (BAS). AIS was identified in 23% (95% CI 8% to 50%) of infants with TGA who underwent BAS, compared with 0% (95% CI 0% to 20%) who did not.ConclusionsCerebral injury in newborns with CHD prior to surgery is common.

Investigating altered brain development in infants with congenital heart disease using tensor-based morphometry

“…A prospective cohort of 74 infants born with critical or serious CHD requiring surgery within one year, based on previously published UK classification 76,77 , was recruited for MR neuroimaging from the Neonatal Intensive Care Unit at St Thomas' Hospital, London. Exclusion criteria were known or suspected genetic syndromes, major abnormalities on MR imaging and GA at birth < 35 weeks.…”

Reduced structural connectivity in cortico-striatal-thalamic network in neonates with congenital heart disease

“…Critical CHD was defined as hypoplastic left heart syndrome, pulmonary atresia with intact ventricular septum, transposition of the great arteries, interruption of the aortic arch and all infants dying or requiring surgery within the first 28 days of life with the following conditions: coarctation of the aorta; aortic valve stenosis; pulmonary valve stenosis; tetralogy of Fallot; pulmonary atresia with ventricular septal defect; total anomalous pulmonary venous connection. Serious CHD was defined as any cardiac lesion not defined as critical, which requires cardiac catheterisation or surgery, or results in death before age one ( Ewer et al, 2011 , Kelly et al, 2019b ). Exclusion criteria included suspected or confirmed chromosomal abnormality or congenital syndrome, neonatal surgery before recruitment (excluding cardiac catherization procedures), suspected congenital infection, or arterial ischaemic infarction on MRI.…”

“…MR images were reported by two neonatal neuroradiologists. All images were subsequently rereviewed to ensure consistency, and lesions classified as focal arterial ischaemic stroke (AIS), white matter injury (WMI), cerebellar haemorrhage or intraventricular haemorrhage as described previously ( Kelly et al, 2019b ). The location and properties of lesions on T1 and T2-weighted imaging, SWI and apparent diffusion coefficient (ADC) map were recorded.…”

“…WMI was classified into normal (no WMI), mild (≤3 foci and all ≤ 2 mm), moderate (>3 and ≤ 10 foci or any > 2 mm) or severe (>10 foci) ( Beca et al, 2013 ). Overall each baby was categorised into one of four brain injury groups; normal, mild (intraventricular haemorrhage, and/or cerebellar haemorrhage ≤ 2 mm, and/or mild WMI), moderate (cerebellar haemorrhage > 2 mm and/or moderate WMI) and severe (severe WMI) ( Kelly et al, 2019b ).…”

“…Magnetic resonance imaging (MRI) studies have identified a high incidence of acquired brain lesions and impaired brain development in infants with CHD ( Glauser et al, 1990 , Miller et al, 2004 , Miller et al, 2007 , Hinton et al, 2008 , Ortinau et al, 2012 , von Rhein et al, 2015 , Kelly et al, 2017 , Kelly et al, 2019a , Kelly et al, 2019b , McQuillen et al, 2006 , Claessens et al, 2016 ). Brain dysmaturation in this population encompasses reduced total and regional brain volume ( Ortinau et al, 2012 , von Rhein et al, 2015 ); impaired cortical gyrification ( Kelly et al, 2017 , Claessens et al, 2016 ) and microstructural development ( Kelly et al, 2019a ); reduced N -acetylaspartate (NAA) to choline ratios and elevated mean diffusivity in deep grey and white matter; and reduced white matter fractional anisotropy ( Miller et al, 2007 ).…”